**1. Introduction**

Inflammatory bowel disease (IBD), consisting primarily of ulcerative colitis (UC) and Crohn's disease (CD), represents a group of chronic inflammatory disorders involving the gastrointestinal tract. Its pathogenesis is complex; however, current research suggests that an intricate network of multiple interacting mechanisms in genetically susceptible individuals may orchestrate the dysregulation of immune and inflammatory responses [1,2].

The transient receptor potential (TRP) channel family, a diverse family of proteins that are reportedly expressed throughout the human body, have emerged as a novel and interrelated system to detect and respond to various environmental stimuli including mechanical, thermal, or chemical stimuli. With this function, they are likely to be sensors for monitoring specific responses to di fferent exogenous and endogenous chemical and physical stimuli [3–6]. Members of the TRP superfamily are

classified according to their amino acid sequences and structural similarities into canonical (TRPC), vanilloid (TRPV), melastatin (TRPM), ankyrin (TRPA), polycystin (TRPP), and mucolipin (TRPML) subfamilies [3–5]. It was recently revealed that the role of TRP channels reaches beyond the control of neuropeptide release from sensory nerves as they are also expressed in immune and resident tissue cells, such as epithelial cells, where they modulate many functions including cytokine production and migration. Therefore, a vital interplay between these cells appears to maintain homeostasis in the intestine, while the disruption of this interplay may be involved in the development and maintenance of IBD [7–10].

In the gu<sup>t</sup> wall of IBD patients, immune cells migrating from systemic circulation release various inflammatory and immunoregulatory molecules, such as cytokines and free radicals, that modulate intestinal inflammation and tissue damage [11]. Therefore, peripheral blood mononuclear cells (PBMCs) are of particular interest due to their involvement in inflammatory and immune cell function. PBMCs may be in contact with multiple stimuli within the blood that have the potential to release TRP channels, resulting in modulation of intestinal inflammation. Therefore, an evaluation of TRP channel expression in PBMCs from IBD patients may provide insights regarding the disease pathogenesis; while changes in their expression level may mirror intestinal inflammation. Recently, the expression of these TRP channel members in PBMCs have been reported in healthy subjects and patients with various diseases [12–15]. However, to date no data regarding their expression in PBMCs from patients with IBD has been reported.

TRPV1–TRPV4; TRPM2, TRPM4, and TRPM5; and TRPC1 as well as TRPC3–TRPC7, are the most relevant TRP channels in immune cells under normal and specific disease conditions [12–15]. Therefore, this study focused on the expression profiles of these TRP channel members in PBMCs obtained from patients with IBD. Furthermore, the relationships between TRP channel levels and the disease activity index, as well as other laboratory parameters were investigated.

#### **2. Materials and Methods**

### *2.1. Ethical Considerations*

This study was approved by the Ethical Committee of Kurume University (14253, 25 March 2015). Written informed consent was obtained from each subject before enrollment in the study.
